scholarly journals Collateral vessel number, plaque burden, and functional decline in peripheral artery disease

2014 ◽  
Vol 19 (4) ◽  
pp. 281-288 ◽  
Author(s):  
Mary M McDermott ◽  
James Carr ◽  
Kiang Liu ◽  
Christopher M Kramer ◽  
Chun Yuan ◽  
...  
Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Elizabeth M Lancaster ◽  
Bian Wu ◽  
Joel Ramirez ◽  
James Iannuzzi ◽  
Michael S Conte ◽  
...  

Introduction: Although data suggests higher rates of functional decline and inferior outcomes in women compared to men after interventions for peripheral artery disease (PAD), women remain underrepresented in contemporary studies. We used a large national database to better understand gender-based differences in presentation and outcomes for patients undergoing endovascular treatment for PAD. Methods: Patients in the Vascular Quality Initiative (VQI) database that underwent lower extremity (LE) endovascular interventions for symptomatic PAD from 2010-2019 were included. Descriptive statistics and multivariable analysis were performed. Results: 128,688 patients (40% female) underwent endovascular LE interventions for symptomatic PAD. Women were more likely to have chronic limb threatening ischemia compared to men (54% vs 51%) and more likely to have a preoperative ABI <0.4 (20% vs 14%). Compared to men, women were older (mean [SD]: 68 [11] vs 70 [12]), more likely to be Black (19% vs 14%), and less likely to be smokers (34% vs 36%), diabetic (50% vs 54%), have CAD (28% vs 35%), or be on dialysis (8% vs 9%) (Table 1). Women were less likely to have exclusively infrapopliteal interventions (8% vs 14%) compared to men (p<0.001 for all). Despite shorter procedural times in women, female gender was an independent predictor of in hospital mortality (OR 1.25, 95% CI 1.09-1.44) in a hierarchical multivariable model adjusting for age, race, smoking, and comorbidities. Women were more likely to be discharged to a rehab or nursing home (11% vs 10%, p< 0.001) and less likely to be taking a statin medication (73% vs 78%, p<0.001). Conclusions: Compared to men, women undergoing endovascular LE interventions for PAD are older, present with more severe disease, and have higher adjusted rates of in hospital mortality. More aggressive screening and medical treatment for PAD in women is needed to address these gender-based differences in disease presentation and clinical outcomes.


2019 ◽  
Vol 24 (5) ◽  
pp. 414-421
Author(s):  
Kerry S Russell ◽  
Denise P Yates ◽  
Christopher M Kramer ◽  
Andrea Feller ◽  
Ping Mahling ◽  
...  

Extensive atherosclerotic plaque burden in the lower extremities often leads to symptomatic peripheral artery disease (PAD) including impaired walking performance and claudication. Interleukin-1β (IL-1β) may play an important pro-inflammatory role in the pathogenesis of this disease. Interruption of IL-1β signaling was hypothesized to decrease plaque progression in the leg macrovasculature and improve the mobility of patients with PAD with intermittent claudication. Thirty-eight patients (mean age 65 years; 71% male) with symptomatic PAD (confirmed by ankle–brachial index) were randomized 1:1 to receive canakinumab (150 mg subcutaneously) or placebo monthly for up to 12 months. The mean vessel wall area (by 3.0 T black-blood magnetic resonance imaging (MRI)) of the superficial femoral artery (SFA) was used to measure plaque volume. Mobility was assessed using the 6-minute walk test. Canakinumab was safe and well tolerated. Markers of systemic inflammation (interleukin-6 and high-sensitivity C-reactive protein) fell as early as 1 month after treatment. MRI (32 patients at 3 months; 21 patients at 12 months) showed no evidence of plaque progression in the SFA in either placebo-treated or canakinumab-treated patients. Although an exploratory endpoint, placebo-adjusted maximum and pain-free walking distance (58 m) improved as early as 3 months after treatment with canakinumab when compared with placebo. Although canakinumab did not alter plaque progression in the SFA, there is an early signal that it may improve maximum and pain-free walking distance in patients with symptomatic PAD. Larger studies aimed at this endpoint will be required to definitively demonstrate this. ClinicalTrials.gov Identifier: NCT01731990


2017 ◽  
Vol 66 (3) ◽  
pp. 826-834 ◽  
Author(s):  
Mary M. McDermott ◽  
Tamar S. Polonsky ◽  
Melina R. Kibbe ◽  
Lu Tian ◽  
Lihui Zhao ◽  
...  

2016 ◽  
Vol 2 (4) ◽  
pp. 00037-2016 ◽  
Author(s):  
Carmen Pizarro ◽  
Fabian Linnhoff ◽  
Fabian van Essen ◽  
Simon Pingel ◽  
Christian Alexander Schaefer ◽  
...  

In view of their common chronic inflammatory process, we sought to determine the linkage between peripheral artery disease and chronic obstructive pulmonary disease (COPD).107 COPD patients (mean±sdage 64.6±10.4 years, 52.2% male) and 22 control smokers without previously diagnosed peripheral artery disease underwent standardised angiological examination for lower extremity artery disease (LEAD) and carotid artery disease.LEAD was significantly more prevalent in COPD patients than in controls (80.4%versus54.5%, p=0.002). Among COPD patients, 57.0%, 12.2%, 10.3% and 0.9% were found to be in Fontaine stages I, IIA, IIB and III, respectively. As with carotid artery disease, its frequency increased from 36.4% in controls to 58.9% in COPD patients (p=0.003). Carotid plaque burden, LEAD Fontaine degrees as well as pulse wave index and ankle–brachial index manifested significant impairment over percentage predicted forced expiratory volume in 1 s (FEV1% pred) (p=0.02, p<0.001, p=0.01 and p<0.001, respectively). Multivariate analysis revealed that COPD Global Initiative for Chronic Obstructive Lung Disease status was the strongest independent predictor for the presence of plaque in lower extremity arteries (odds ratio 1.63, 95% CI 1.19–2.25, p=0.003) and carotids (odds ratio 1.66, 95% CI 1.14–2.44, p=0.009).As compared with control smokers, peripheral artery disease is diagnosed in a sizeable proportion of COPD patients and exhibits significant distributive differences over FEV1% pred that exceed the susceptibility conferred by common cardiovascular stressors.


2021 ◽  
Author(s):  
Seyedeh M. Zekavat ◽  
Vanesa Viana-Huete ◽  
María A. Zuriaga ◽  
Md Mesbah Uddin ◽  
Mark Trinder ◽  
...  

AbstractBackgroundSomatic mutations in blood indicative of clonal hematopoiesis of indeterminate potential (CHIP), particularly in DNMT3A, TET2, and JAK2, are associated with an increased risk of hematologic malignancy, coronary artery disease, and all-cause mortality. However, whether CHIP is associated with increased risk of peripheral artery disease (PAD) remains unknown. In addition, chemotherapy frequently causes mutations in DNA Damage Repair (DDR) genes TP53 and PPM1D, and whether CHIP caused by somatic mutations in DDR genes results in increased risk of atherosclerosis is unclear. We sought to test whether CHIP, and CHIP caused by DDR genes, associates with incident peripheral artery disease (PAD) and atherosclerosis.MethodsWe identified CHIP among 50,122 exome sequences in individuals from UK and Mass General Brigham Biobanks and tested CHIP status (N=2,851) with incident PAD and atherosclerosis across multiple arterial beds. To mimic the human scenario of clonal hematopoiesis and test whether the expansion of p53-deficient hematopoietic cells contributes to atherosclerosis, a competitive bone marrow transplantation (BMT) strategy was used to generate atherosclerosis-prone Ldlr-/- chimeric mice carrying 20% Trp53-/- hematopoietic cells (20% KO-BMT mice). We then evaluated aortic plaque burden and plaque macrophage accumulation 12 weeks after grafting.ResultsCHIP associated with incident PAD (HR 1.7; P=2.2x10-5) and atherosclerosis in multiple beds (HR 1.3; P=9.7x10-5), with increased risk among individuals with DDR CHIP (HR 2.0; P=0.0084). Among atherosclerosis-prone Ldlr null mice, the p53 -/- 20% KO-BMT mice demonstrated increased aortic plaque size (p=0.013) and accumulation of p53-/- plaque macrophages (P<0.001), driven by an abundance of p53-deficient plaque macrophages. The expansion of p53-deficient cells did not affect the expression of the pro-inflammatory cytokines IL-6 and IL-1β in the atherosclerotic aortic wall.ConclusionsOur findings highlight the role of CHIP as a broad driver of atherosclerosis across the entire arterial system, with evidence of increased plaque among p53 -/- 20% KO-BMT mice via expansion of plaque macrophages. These observations provide new insight into the link between CHIP and cardiovascular disease, and lend human genetic support to the concept that post-cytotoxic chemotherapy patients may benefit from surveillance for atherosclerotic conditions in addition to therapy-related myeloid neoplasms.


2014 ◽  
Vol 19 (1) ◽  
pp. 18-26 ◽  
Author(s):  
Mary M McDermott ◽  
Kiang Liu ◽  
Luigi Ferrucci ◽  
Lu Tian ◽  
Jack Guralnik ◽  
...  

VASA ◽  
2017 ◽  
Vol 46 (3) ◽  
pp. 151-158 ◽  
Author(s):  
Hisato Takagi ◽  
Takuya Umemoto

Abstract. Both coronary and peripheral artery disease are representative atherosclerotic diseases, which are also known to be positively associated with presence of abdominal aortic aneurysm. It is still controversial, however, whether coronary and peripheral artery disease are positively associated with expansion and rupture as well as presence of abdominal aortic aneurysm. In the present article, we overviewed epidemiological evidence, i. e. meta-analyses, regarding the associations of coronary and peripheral artery disease with presence, expansion, and rupture of abdominal aortic aneurysm through a systematic literature search. Our exhaustive search identified seven meta-analyses, which suggest that both coronary and peripheral artery disease are positively associated with presence of abdominal aortic aneurysm, may be negatively associated with expansion of abdominal aortic aneurysm, and might be unassociated with rupture of abdominal aortic aneurysm.


Sign in / Sign up

Export Citation Format

Share Document